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1.
Schizophr Res ; 240: 143-149, 2022 02.
Article in English | MEDLINE | ID: mdl-35026599

ABSTRACT

OBJECTIVE: Sex differences in schizophrenia have been noted across domains such as sleep and cognitive function; however, how they interact remains unclear. This study aimed to explore sex differences in the relationship between insomnia and cognitive function in patients with chronic schizophrenia. METHODS: 718 schizophrenia patients (480 males and 238 females) and 397 healthy controls were recruited. Insomnia was collected by a questionnaire. Insomnia severity index (ISI) was used to evaluate the severity of insomnia. The clinical symptoms and cognition were assessed with the Positive and Negative Syndrome Scale (PANSS) and the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS), respectively. RESULTS: Schizophrenia patients showed significantly lower scores compared to healthy controls on the RBANS total score and four indexes (all p < 0.05). Male patients had a lower rate of insomnia, higher scores on the RBANS visuospatial/constructional, language, and total score than female patients (all P < 0.05). Insomnia patients had lower RBANS immediate memory, language, and total scores than non-insomnia patients, and the results only appeared in female patients (all P < 0.05). In addition, there were significant negative correlations between ISI and RBANS language and delayed memory in male patients, while ISI was significantly negatively correlated with RBANS immediate memory in female patients (all P < 0.05). CONCLUSION: Our findings suggest that there are sex differences in insomnia, cognitive performance, and their association in patients with chronic schizophrenia. These sex differences may have important potential clinical significance for the identification, evaluation, and treatment of insomnia in patients with chronic schizophrenia.


Subject(s)
Cognitive Dysfunction , Schizophrenia , Sleep Initiation and Maintenance Disorders , Cognitive Dysfunction/epidemiology , Cognitive Dysfunction/etiology , Female , Humans , Male , Neuropsychological Tests , Schizophrenia/complications , Schizophrenia/diagnosis , Schizophrenia/epidemiology , Schizophrenic Psychology , Sex Characteristics , Sleep Initiation and Maintenance Disorders/epidemiology
2.
Sci Rep ; 10(1): 5008, 2020 03 19.
Article in English | MEDLINE | ID: mdl-32193498

ABSTRACT

Patients with schizophrenia (SCZ) exhibit higher suicide rates than the general population. However, the molecular mechanism responsible for the high rate of suicidal behavior in SCZ remains poorly understood. MTHFR Ala222Val (C677T; rs 1801133) polymorphism has repeatedly demonstrated to play a pathological role in numerous mental disorders, but none of these studies focused on the susceptibility of suicidal behavior in SCZ. In the present cross-sectional study, we recruited 957 chronic inpatients with SCZ and 576 healthy controls to assess the psychopathological symptoms of SCZ and compare the frequency of the MTHFR Ala222Val genotype in both suicide attempters and non-attempters. Our results demonstrated no significant differences in MTHFR Ala222Val genotype and allele distributions between the SCZ patients and controls (p > 0.05), but showed a statistical significance in the distribution of Ala/Val genotype between suicide attempters and non-attempters (p < 0.05). Further logistic regression analysis showed that MTHFR Ala222Val genotype, psychopathological symptoms, number of cigarettes smoked per day and drinking status were related to suicide attempts in SCZ (p < 0.05). Our study demonstrated that MTHFR Ala222Val polymorphism and some clinical characteristics might confer susceptibility to suicide in patients with SCZ.


Subject(s)
Genetic Predisposition to Disease/genetics , Methylenetetrahydrofolate Reductase (NADPH2)/genetics , Polymorphism, Genetic , Schizophrenia/genetics , Schizophrenic Psychology , Suicide, Attempted , Adult , Alcohol Drinking/adverse effects , Chronic Disease , Cigarette Smoking/adverse effects , Cross-Sectional Studies , Female , Humans , Male , Middle Aged
3.
Psychiatry Res ; 257: 279-283, 2017 11.
Article in English | MEDLINE | ID: mdl-28783576

ABSTRACT

The neurotrophic hypothesis of depression is supported by consistent findings of lower serum BDNF levels in depressed patients. Increasing evidence shows different clinical characteristics of patients with psychotic major depression versus nonpsychotic major depression. However, the possible association between BDNF and psychotic symptoms in depression has not been investigated. We recruited 90 treatment-resistant depression (TRD) patients and 90 gender- and age-matched healthy control subjects and examined serum BDNF in both groups. Patients' depressive symptoms were assessed using the 17-item Hamilton Depression Rating Scale (HDRS-17), and psychopathological symptoms by the 18-item Brief Psychiatric Rating Scale (BPRS-18). Our results showed that BDNF levels were significantly lower in patients than controls. Correlation analysis revealed a significantly positive correlation between BDNF and the thought disturbance subscale of BPRS-18 (p < 0.05), and a trend toward a significantly positive correlation between BDNF and the BPRS-18 total score (p = 0.06). Stepwise multiple regression analyses confirmed BDNF as the influencing factor for the thought disturbance subscales of the BPRS-18. Our findings suggest that BDNF may be involved in the pathophysiology of TRD, and its associated psychotic symptoms, especially thought disturbance.


Subject(s)
Brain-Derived Neurotrophic Factor/blood , Depressive Disorder, Treatment-Resistant/blood , Depressive Disorder, Treatment-Resistant/psychology , Psychotic Disorders/blood , Psychotic Disorders/psychology , Adult , Asian People/psychology , Brief Psychiatric Rating Scale , Case-Control Studies , China/ethnology , Female , Humans , Male , Middle Aged , Regression Analysis
4.
Schizophr Res ; 2006 Jul 17.
Article in English | MEDLINE | ID: mdl-16846718

ABSTRACT

This article has been removed, consistent with Elsevier Policy on Article Withdrawal. Please see http://www.elsevier.com/locate/withdrawalpolicy. The Publisher apologizes for any inconvenience this may cause.

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